Non-Alcoholic Fatty Liver Disease Information for Patients

Total Page:16

File Type:pdf, Size:1020Kb

Non-Alcoholic Fatty Liver Disease Information for Patients April 2021 | www.hepatitis.va.gov Non-Alcoholic Fatty Liver Disease Information for Patients What is Non-Alcoholic Fatty Liver Disease? Losing more than 10% of your body weight can improve liver inflammation and scarring. Make a weight loss plan Non-alcoholic fatty liver disease or NAFLD is when fat is with your provider— and exercise to keep weight off. increased in the liver and there is not a clear cause such as excessive alcohol use. The fat deposits can cause liver damage. Exercise NAFLD is divided into two types: simple fatty liver and non- Start small, with a 5-10 minute brisk walk for example, alcoholic steatohepatitis (NASH). Most people with NAFLD and gradually build up. Aim for 30 minutes of moderate have simple fatty liver, however 25-30% have NASH. With intensity exercise on most days of the week (150 minutes/ NASH, there is inflammation and scarring of the liver. A small week). The MOVE! Program is a free VA program to help number of people will develop significant scarring in their lose weight and keep it off. liver, called cirrhosis. Avoid Alcohol People with NAFLD often have one or more features of Minimize alcohol as much as possible. If you do drink, do metabolic syndrome: obesity, high blood pressure, low HDL not drink more than 1-2 drinks a day. Patients with cirrhosis cholesterol, insulin resistance or diabetes. of the liver should not drink alcohol at all. NAFLD increases the risk for diabetes, cardiovascular disease, Treat high blood sugar and high cholesterol and kidney disease. Ask your provider if you have high blood sugar or high Most people feel fine and have no symptoms. Currently, there cholesterol. Certain medications can help lower blood are no FDA-approved medications to treat NAFLD. However, sugar levels and cholesterol. several medicines are being studied in clinical trials. What if I have NAFLD and another How will I know if I have NAFLD? liver disease? Talk to your health provider about screening for NAFLD if People can have fatty liver and other liver diseases— such you have type two diabetes. Your provider may perform as hepatitis C. People who drink alcohol over many years radiology tests (such as ultrasound). A non-invasive test called can also develop alcoholic liver disease including cirrhosis. FibroScan® may be used to meassure the amount of fat in Having two liver diseases can cause more liver injury and your liver and to look for fibrosis (scarring) in your liver. Some scarring, so it’s even more important to lose weight and people may need a liver biopsy. exercise—to decrease liver fat and injury. And be sure What can I do if I have NAFLD? to talk to your provider about treatment for other liver diseases as well. Lose weight Weight loss is the best treatment. Comprehensive lifestyle Resources modification, which includes changes in diet and increase in NAFLD patient guide and video: https://www.hepatitis.va.gov/ exercise, has the greatest, longest lasting weight loss benefit. MOVE! Weight Management Program: www.move.va.gov The good news is that NAFLD can be reversed if you lose more than 4% of your body weight. For example: • 8 pounds or more (if you’re 200 pounds) • 12 pounds or more (if you’re 300 pounds).
Recommended publications
  • Steatosis in Hepatitis C: What Does It Mean? Tarik Asselah, MD, Nathalie Boyer, MD, and Patrick Marcellin, MD*
    Steatosis in Hepatitis C: What Does It Mean? Tarik Asselah, MD, Nathalie Boyer, MD, and Patrick Marcellin, MD* Address Steatosis *Service d’Hépatologie, Hôpital Beaujon, Mechanisms of steatosis 100 Boulevard du Général Leclerc, Clichy 92110, France. Hepatic steatosis develops in the setting of multiple E-mail: [email protected] clinical conditions, including obesity, diabetes mellitus, Current Hepatitis Reports 2003, 2:137–144 alcohol abuse, protein malnutrition, total parenteral Current Science Inc. ISSN 1540-3416 Copyright © 2003 by Current Science Inc. nutrition, acute starvation, drug therapy (eg, corticosteroid, amiodarone, perhexiline, estrogens, methotrexate), and carbohydrate overload [1–4,5••]. Hepatitis C and nonalcoholic fatty liver disease (NAFLD) are In the fed state, dietary triglycerides are processed by the both common causes of liver disease. Thus, it is not surprising enterocyte into chylomicrons, which are secreted into the that they can coexist in the same individual. The prevalence of lymph. The chylomicrons are hydrolyzed into fatty acids by steatosis in patients with chronic hepatitis C differs between lipoprotein lipase. These free fatty acids are transported to the studies, probably reflecting population differences in known liver, stored in adipose tissue, or used as energy sources by risk factors for steatosis, namely overweight, diabetes, and muscles. Free fatty acids are also supplied to the liver in the dyslipidemia. The pathogenic significance of steatosis likely form of chylomicron remnants, which are then hydrolyzed by differs according to its origin, metabolic (NAFLD or non- hepatic triglyceride lipase. During fasting, the fatty acids sup- alcoholic steatohepatitis) or virus related (due to hepatitis C plied to the liver are derived from hydrolysis (mediated by a virus genotype 3).
    [Show full text]
  • Chronic Viral Hepatitis in a Cohort of Inflammatory Bowel Disease
    pathogens Article Chronic Viral Hepatitis in a Cohort of Inflammatory Bowel Disease Patients from Southern Italy: A Case-Control Study Giuseppe Losurdo 1,2 , Andrea Iannone 1, Antonella Contaldo 1, Michele Barone 1 , Enzo Ierardi 1 , Alfredo Di Leo 1,* and Mariabeatrice Principi 1 1 Section of Gastroenterology, Department of Emergency and Organ Transplantation, University “Aldo Moro” of Bari, 70124 Bari, Italy; [email protected] (G.L.); [email protected] (A.I.); [email protected] (A.C.); [email protected] (M.B.); [email protected] (E.I.); [email protected] (M.P.) 2 Ph.D. Course in Organs and Tissues Transplantation and Cellular Therapies, Department of Emergency and Organ Transplantation, University “Aldo Moro” of Bari, 70124 Bari, Italy * Correspondence: [email protected]; Tel.: +39-080-559-2925 Received: 14 September 2020; Accepted: 21 October 2020; Published: 23 October 2020 Abstract: We performed an epidemiologic study to assess the prevalence of chronic viral hepatitis in inflammatory bowel disease (IBD) and to detect their possible relationships. Methods: It was a single centre cohort cross-sectional study, during October 2016 and October 2017. Consecutive IBD adult patients and a control group of non-IBD subjects were recruited. All patients underwent laboratory investigations to detect chronic hepatitis B (HBV) and C (HCV) infection. Parameters of liver function, elastography and IBD features were collected. Univariate analysis was performed by Student’s t or chi-square test. Multivariate analysis was performed by binomial logistic regression and odds ratios (ORs) were calculated. We enrolled 807 IBD patients and 189 controls. Thirty-five (4.3%) had chronic viral hepatitis: 28 HCV (3.4%, versus 5.3% in controls, p = 0.24) and 7 HBV (0.9% versus 0.5% in controls, p = 0.64).
    [Show full text]
  • Zoonotic Diseases Fact Sheet
    ZOONOTIC DISEASES FACT SHEET s e ion ecie s n t n p is ms n e e s tio s g s m to a a o u t Rang s p t tme to e th n s n m c a s a ra y a re ho Di P Ge Ho T S Incub F T P Brucella (B. Infected animals Skin or mucous membrane High and protracted (extended) fever. 1-15 weeks Most commonly Antibiotic melitensis, B. (swine, cattle, goats, contact with infected Infection affects bone, heart, reported U.S. combination: abortus, B. suis, B. sheep, dogs) animals, their blood, tissue, gallbladder, kidney, spleen, and laboratory-associated streptomycina, Brucellosis* Bacteria canis ) and other body fluids causes highly disseminated lesions bacterial infection in tetracycline, and and abscess man sulfonamides Salmonella (S. Domestic (dogs, cats, Direct contact as well as Mild gastroenteritiis (diarrhea) to high 6 hours to 3 Fatality rate of 5-10% Antibiotic cholera-suis, S. monkeys, rodents, indirect consumption fever, severe headache, and spleen days combination: enteriditis, S. labor-atory rodents, (eggs, food vehicles using enlargement. May lead to focal chloramphenicol, typhymurium, S. rep-tiles [especially eggs, etc.). Human to infection in any organ or tissue of the neomycin, ampicillin Salmonellosis Bacteria typhi) turtles], chickens and human transmission also body) fish) and herd animals possible (cattle, chickens, pigs) All Shigella species Captive non-human Oral-fecal route Ranges from asymptomatic carrier to Varies by Highly infective. Low Intravenous fluids primates severe bacillary dysentery with high species. 16 number of organisms and electrolytes, fevers, weakness, severe abdominal hours to 7 capable of causing Antibiotics: ampicillin, cramps, prostration, edema of the days.
    [Show full text]
  • Primary Biliary Cholangitis: a Brief Overview Justin S
    REVIEW Primary Biliary Cholangitis: A Brief Overview Justin S. Louie,* Sirisha Grandhe,* Karen Matsukuma,† and Christopher L. Bowlus* Primary biliary cholangitis (PBC), previously referred to supported by the higher concordance of PBC in monozy- as primary biliary cirrhosis, is the most common chronic gotic compared with dizygotic twins.4 In addition, certain cholestatic autoimmune disease affecting adults in the human leukocyte antigen haplotypes have been associ- United States.1 It is characterized by a hallmark serologic ated with PBC, as well as variants at loci along the inter- signature, antimitochondrial antibody (AMA), and specific leukin-12 (IL-12) immunoregulatory pathway (IL-12A and bile duct pathology with progressive intrahepatic duct de- IL-12RB2 loci).5 struction leading to cholestasis. PBC is potentially fatal and can have both intrahepatic and extrahepatic complications. PATHOGENESIS EPIDEMIOLOGY The primary disease mechanism in PBC is thought to be T cell lymphocyte–mediated injury against intralobu- PBC affects all races and ethnicities; however, it is best lar biliary epithelial cells. This causes progressive destruc- studied in the Caucasian population. The condition pre- tion and eventual disappearance of the intralobular bile dominantly affects women older than 40 years, with a ducts. Molecular mimicry has been proposed as the ini- female/male ratio of 9:1.2 Although the incidence of PBC tiating event in the loss of tolerance primarily to mito- appears to be stable, the overall prevalence of the disease chondrial pyruvate dehydrogenase complex, E2, during is increasing.3 An individual’s genetic susceptibility, epige- which exogenous antigens evoke an immune response netic factors, and certain environmental triggers seem to that recognizes an endogenous (self) antigen inciting an play important roles.
    [Show full text]
  • Hepatitis A, B, and C: Learn the Differences
    Hepatitis A, B, and C: Learn the Differences Hepatitis A Hepatitis B Hepatitis C caused by the hepatitis A virus (HAV) caused by the hepatitis B virus (HBV) caused by the hepatitis C virus (HCV) HAV is found in the feces (poop) of people with hepa- HBV is found in blood and certain body fluids. The virus is spread HCV is found in blood and certain body fluids. The titis A and is usually spread by close personal contact when blood or body fluid from an infected person enters the body virus is spread when blood or body fluid from an HCV- (including sex or living in the same household). It of a person who is not immune. HBV is spread through having infected person enters another person’s body. HCV can also be spread by eating food or drinking water unprotected sex with an infected person, sharing needles or is spread through sharing needles or “works” when contaminated with HAV. “works” when shooting drugs, exposure to needlesticks or sharps shooting drugs, through exposure to needlesticks on the job, or from an infected mother to her baby during birth. or sharps on the job, or sometimes from an infected How is it spread? Exposure to infected blood in ANY situation can be a risk for mother to her baby during birth. It is possible to trans- transmission. mit HCV during sex, but it is not common. • People who wish to be protected from HAV infection • All infants, children, and teens ages 0 through 18 years There is no vaccine to prevent HCV.
    [Show full text]
  • Active Peptic Ulcer Disease in Patients with Hepatitis C Virus-Related Cirrhosis: the Role of Helicobacter Pylori Infection and Portal Hypertensive Gastropathy
    dore.qxd 7/19/2004 11:24 AM Page 521 View metadata, citation and similar papers at core.ac.uk ORIGINAL ARTICLE brought to you by CORE provided by Crossref Active peptic ulcer disease in patients with hepatitis C virus-related cirrhosis: The role of Helicobacter pylori infection and portal hypertensive gastropathy Maria Pina Dore MD PhD, Daniela Mura MD, Stefania Deledda MD, Emmanouil Maragkoudakis MD, Antonella Pironti MD, Giuseppe Realdi MD MP Dore, D Mura, S Deledda, E Maragkoudakis, Ulcère gastroduodénal évolutif chez les A Pironti, G Realdi. Active peptic ulcer disease in patients patients atteints de cirrhose liée au HCV : Le with hepatitis C virus-related cirrhosis: The role of Helicobacter pylori infection and portal hypertensive rôle de l’infection à Helicobacter pylori et de la gastropathy. Can J Gastroenterol 2004;18(8):521-524. gastropathie liée à l’hypertension portale BACKGROUND & AIM: The relationship between Helicobacter HISTORIQUE ET BUT : Le lien entre l’infection à Helicobacter pylori pylori infection and peptic ulcer disease in cirrhosis remains contro- et l’ulcère gastroduodénal dans la cirrhose reste controversé. Le but de la versial. The purpose of the present study was to investigate the role of présente étude est de vérifier le rôle de l’infection à H. pylori et de la gas- H pylori infection and portal hypertension gastropathy in the preva- tropathie liée à l’hypertension portale dans la prévalence de l’ulcère gas- lence of active peptic ulcer among dyspeptic patients with compen- troduodénal évolutif chez les patients dyspeptiques souffrant d’une sated hepatitis C virus (HCV)-related cirrhosis.
    [Show full text]
  • Understanding Human Astrovirus from Pathogenesis to Treatment
    University of Tennessee Health Science Center UTHSC Digital Commons Theses and Dissertations (ETD) College of Graduate Health Sciences 6-2020 Understanding Human Astrovirus from Pathogenesis to Treatment Virginia Hargest University of Tennessee Health Science Center Follow this and additional works at: https://dc.uthsc.edu/dissertations Part of the Diseases Commons, Medical Sciences Commons, and the Viruses Commons Recommended Citation Hargest, Virginia (0000-0003-3883-1232), "Understanding Human Astrovirus from Pathogenesis to Treatment" (2020). Theses and Dissertations (ETD). Paper 523. http://dx.doi.org/10.21007/ etd.cghs.2020.0507. This Dissertation is brought to you for free and open access by the College of Graduate Health Sciences at UTHSC Digital Commons. It has been accepted for inclusion in Theses and Dissertations (ETD) by an authorized administrator of UTHSC Digital Commons. For more information, please contact [email protected]. Understanding Human Astrovirus from Pathogenesis to Treatment Abstract While human astroviruses (HAstV) were discovered nearly 45 years ago, these small positive-sense RNA viruses remain critically understudied. These studies provide fundamental new research on astrovirus pathogenesis and disruption of the gut epithelium by induction of epithelial-mesenchymal transition (EMT) following astrovirus infection. Here we characterize HAstV-induced EMT as an upregulation of SNAI1 and VIM with a down regulation of CDH1 and OCLN, loss of cell-cell junctions most notably at 18 hours post-infection (hpi), and loss of cellular polarity by 24 hpi. While active transforming growth factor- (TGF-) increases during HAstV infection, inhibition of TGF- signaling does not hinder EMT induction. However, HAstV-induced EMT does require active viral replication.
    [Show full text]
  • Hepatitis C 2005 Clinical Guidelines Summary of The: New York State Department of Health Clinical Guidelines for the Medical Management of Hepatitis C
    Hepatitis C 2005 Clinical Guidelines Summary of the: New York State Department of Health Clinical Guidelines for the Medical Management of Hepatitis C Inside: Key Features of Viral Hepatitis A,B and C 1 Natural Course of HCV Infection 2 Persons at Risk for HCV Infection 3 Sources of HCV Infection 4 Counseling Prior To Testing 5 Screening for HCV Algorithm 6 Laboratory Testing for HCV 7 Interpretation of HCV Test Results 8 Post Exposure Screening for HCV 9 Counseling After Testing 10 Treating HCV Patients 11 Medical Management of HCV Positive Patients 12 References and Internet Resources 13 Hepatitis C Virus The Hidden Epidemic The Burden of HCV • 3 million Americans are chronically infected with the • 8-10,000 deaths a year are caused by HCV. Hepatitis C virus (HCV). • HCV is the leading cause for liver transplants and • 342,000 New Yorkers are estimated to be infected chronic liver disease. with HCV. • HCV deaths will increase four-fold to 38,000, by • A majority of the people infected with HCV do not the year 2010. know they have it. • Years of life lost to Hepatitis C (2001-2019) • Thousands of people go undetected each year—due 3.1 million years to inadequate risk assessment, under-screening and confusion about the use of diagnostic tests. • Cost of premature disability and death (2010-2109) $75.5 billion Hepatitis C Virus • Direct medical costs in absentee losses due to Hepatitis C $750 million/ year • HCV is a blood-borne disease transmitted by • Total medical expenditures for persons with HCV blood-to-blood contact.
    [Show full text]
  • Hepatitis C Virus Infection and Human Pancreatic ß-Cell Dysfunction
    Pathophysiology/Complications BRIEF REPORT Hepatitis C Virus Infection and Human Pancreatic ␤-Cell Dysfunction 1 1 MATILDE MASINI, MD SILVIA DEL GUERRA, PHD showing the characteristic insulin gran- 2 1 DANIELA CAMPANI, MD MARCO BUGLIANI, PHD ules and normally preserved mitochon- 3 1 UGO BOGGI, MD SCILLA TORRI, PHD ␤ 2 1 dria. In -cells from HCV-positive MICHELE MENICAGLI, MD STEFANO DEL PRATO, MD 1 3 pancreases, the presence of virus-like par- NICOLA FUNEL, MD FRANCO MOSCA, MD 1 4 ticles was observed, mainly close to the MARIA POLLERA, MD FRANCO FILIPPONI, MD 1 1 membranes of Golgi apparatus, which, in ROBERTO LUPI, PHD PIERO MARCHETTI, MD, PHD turn, appeared hyperplastic and dilated (Fig. 1D). The mitochondria appeared round-shaped with dispersed matrix and fragmented cristae (Fig. 1D). Additional Ϯ 2 any patients with chronic hepati- and 2 women, BMI 25.8 1.6 kg/m ) ␤-cell changes were observed at the Ϯ tis C virus (HCV) develop type 2 and 10 HCV-negative (age 67 9 years, level of rough endoplasmic reticulum, Ϯ diabetes (1). This prevalence is 6 men and 4 women, BMI 26.8 2.0 which showed long and dilated tubular M 2 much higher than that observed in the kg/m ) donors were harvested and stud- membranes, with numerous electron- general population and in patients with ied with the approval of our local ethics dense ribosomes bound to the latter (not other chronic liver diseases such as hepa- committee. Histological studies were shown). These morphological changes titis B virus, alcoholic liver disease, and performed by immunohistochemistry were accompanied by reduced in vitro primary biliary cirrhosis.
    [Show full text]
  • Non-Alcoholic Fatty Liver Disease
    Non-alcoholic fatty liver disease Description Non-alcoholic fatty liver disease (NAFLD) is a buildup of excessive fat in the liver that can lead to liver damage resembling the damage caused by alcohol abuse, but that occurs in people who do not drink heavily. The liver is a part of the digestive system that helps break down food, store energy, and remove waste products, including toxins. The liver normally contains some fat; an individual is considered to have a fatty liver (hepatic steatosis) if the liver contains more than 5 to 10 percent fat. The fat deposits in the liver associated with NAFLD usually cause no symptoms, although they may cause increased levels of liver enzymes that are detected in routine blood tests. Some affected individuals have abdominal pain or fatigue. During a physical examination, the liver may be found to be slightly enlarged. Between 7 and 30 percent of people with NAFLD develop inflammation of the liver (non- alcoholic steatohepatitis, also known as NASH), leading to liver damage. Minor damage to the liver can be repaired by the body. However, severe or long-term damage can lead to the replacement of normal liver tissue with scar tissue (fibrosis), resulting in irreversible liver disease (cirrhosis) that causes the liver to stop working properly. Signs and symptoms of cirrhosis, which get worse as fibrosis affects more of the liver, include fatigue, weakness, loss of appetite, weight loss, nausea, swelling (edema), and yellowing of the skin and whites of the eyes (jaundice). Scarring in the vein that carries blood into the liver from the other digestive organs (the portal vein) can lead to increased pressure in that blood vessel (portal hypertension), resulting in swollen blood vessels (varices) within the digestive system.
    [Show full text]
  • Vaccinations for Adults with Chronic Liver Disease Or Infection
    Vaccinations for Adults with Chronic Liver Disease or Infection This table shows which vaccinations you should have to protect your health if you have chronic hepatitis B or C infection or chronic liver disease (e.g., cirrhosis). Make sure you and your healthcare provider keep your vaccinations up to date. Vaccine Do you need it? Hepatitis A Yes! Your chronic liver disease or infection puts you at risk for serious complications if you get infected with the (HepA) hepatitis A virus. If you’ve never been vaccinated against hepatitis A, you need 2 doses of this vaccine, usually spaced 6–18 months apart. Hepatitis B Yes! If you already have chronic hepatitis B infection, you won’t need hepatitis B vaccine. However, if you have (HepB) hepatitis C or other causes of chronic liver disease, you do need hepatitis B vaccine. The vaccine is given in 2 or 3 doses, depending on the brand. Ask your healthcare provider if you need screening blood tests for hepatitis B. Hib (Haemophilus Maybe. Some adults with certain high-risk conditions, for example, lack of a functioning spleen, need vaccination influenzae type b) with Hib. Talk to your healthcare provider to find out if you need this vaccine. Human Yes! You should get this vaccine if you are age 26 years or younger. Adults age 27 through 45 may also be vacci- papillomavirus nated against HPV after a discussion with their healthcare provider. The vaccine is usually given in 3 doses over a (HPV) 6-month period. Influenza Yes! You need a dose every fall (or winter) for your protection and for the protection of others around you.
    [Show full text]
  • Hepatitis a Reporting Guideline
    Hepatitis A Signs and • Abrupt onset of fever, headache, malaise, anorexia, vomiting, diarrhea, abdominal pain Symptoms • Jaundice • Rare fatalities, particularly risk if chronic liver disease including chronic hepatitis B or C • Younger children and very rare adults may have asymptomatic infection Incubation 15–50 days, with an average of 30 days Case Clinical: acute illness, discrete onset of a consistent symptoms (fever, headache, nausea, diarrhea, classification anorexia, vomiting, abdominal pain) and either jaundice (bilirubin ≥ 3.0) or elevated ALT (≥ 200) Confirmed: Clinical & either IgM or PCR positive OR clinical with epi link to a confirmed case Differential Hepatitis B or C (do tests), chemical hepatitis (e.g., alcohol, some medications, natural products), diagnosis autoimmune hepatitis, biliary disease (gallstones), malignancy, metabolic (e.g., Wilson’s) Treatment Supportive Duration Illness may be prolonged or relapse for months with continued virus excretion; communicable before onset until asymptomatic although longer excretion in children and if relapses Exposures Contaminated food or water, particularly during travel; contact with a case (household, sexual) Laboratory • Serologic testing is available commercially; CDC genotypes for outbreak Testing • Spin serum, separate, freeze, send to PHL. CDE will complete special CDC manifest. See: https://www.cdc.gov/laboratory/specimen-submission/pdf/form-50-34.pdf. Public • Identify potential sources of exposure: close contact with acute hepatitis A case, restaurant or Health
    [Show full text]